Synaptic plasticity may underlie l -DOPA induced dyskinesia

Abstract

<p class="first" id="P1">L-DOPA provides highly effective treatment for Parkinson’s disease, but L-DOPA induced dyskinesia (LID) is a very debilitating response that eventually is presented by a majority of patients. A central issue in understanding the basis of LID is whether it is due to a response to chronic L-DOPA over years of therapy, and/or due to synaptic changes that follow the loss of dopaminergic neurotransmission and then triggered by acute L-DOPA administration. We review recent work that suggests that specific synaptic changes in the D1 dopamine receptor-expressing direct pathway striatal projection neurons due to loss of dopamine in Parkinson’s disease are responsible for LID. Chronic L-DOPA may nevertheless modulate LID through priming mechanisms. </p>